Mechanism of Ikaros tumor suppression in Leukemia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA189192 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5312350.fastq.gz | Fastqsanger.gz | |||
| SRR5312351.fastq.gz | Fastqsanger.gz | |||
| SRR708089.fastq.gz | Fastqsanger.gz | |||
| SRR708090.fastq.gz | Fastqsanger.gz | |||
| SRR708091.fastq.gz | Fastqsanger.gz |
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Project description:Ikaros functions as a master regulator of lymphocyte differentiation and a tumor suppressor. Ikaros binds DNA and regulates gene expression by chromatin remodeling. Mechanisms of Ikaros-mediated tumor suppression are unknown. Here we examined genome-wide occupancy of Ikaros and histone deacetylase 1 (HDAC1) and Histone midificaition markers in human leukemia, and found that the Ikaros and HDAC1 showed similar binding partern and HDAC1âDNA interactions are associated with the presence of bivalent chromatin, and the recruitment of HDAC1 by Ikaros is associated with bivalent chromatin at Ikaros target genes. Examine the genome-wide binding of Ikaros, HDAC1, H3K9me3, H3K9ac, H3K27me3, H3K4me3 and H3K36me3 in Nalm6 ALL leukemia cells.
2015-11-03 | E-GEOD-44217 | biostudies-arrayexpress
Project description:Ikaros functions as a master regulator of lymphocyte differentiation and a tumor suppressor. Ikaros binds DNA and regulates gene expression by chromatin remodeling. Mechanisms of Ikaros-mediated tumor suppression are unknown. Here we examined genome-wide occupancy of Ikaros and histone deacetylase 1 (HDAC1) and Histone midificaition markers in human leukemia, and found that the Ikaros and HDAC1 showed similar binding partern and HDAC1–DNA interactions are associated with the presence of bivalent chromatin, and the recruitment of HDAC1 by Ikaros is associated with bivalent chromatin at Ikaros target genes.
2015-11-03 | GSE44217 | GEO
Project description:Ikaros tumor suppression and epigenetic regulation
| PRJNA522391 | ENA
Project description:Ikaros encodes a transcription factor that functions as a tumor suppressor in T-ALL. The mechanisms through which Ikaros regulates gene expression and cellular proliferation in T-ALL are unknown. Re-introduction of Ikaros into Ikaros-null T-ALL cells results in cessation of cellular proliferation and induction of T-cell differentiation. We performed dynamic global epigenomic and gene expression analyses to determine the role of Ikaros in tumor suppression during this process. Our results identified novel Ikaros functions in the epigenetic regulation of gene expression: Ikaros directly regulates de novo formation and depletion of enhancers, as well as de novo formation of active enhancers and activation of poised enhancers; Ikaros directly induces the formation of super-enhancers; and Ikaros demonstrates pioneering activity by directly regulating chromatin accessibility. Dynamic analyses demonstrate the long-lasting effect of Ikaros DNA binding on enhancer activation, de novo formation of enhancers and super-enhancers, and chromatin accessibility. Ikaros induces profound, global re-distribution of HDAC1 via recruitment of HDAC1 to promoter and enhancer regions of different target genes. Expression analysis identified a large number of novel signaling pathways that are directly regulated by Ikaros and Ikaros-induced enhancers, and that are responsible for the cessation of proliferation and induction of T-cell differentiation in T-ALL cells.
2019-03-31 | GSE126568 | GEO
Project description:Ikaros encodes a transcription factor that functions as a tumor suppressor in T-ALL. The mechanisms through which Ikaros regulates gene expression and cellular proliferation in T-ALL are unknown. Re-introduction of Ikaros into Ikaros-null T-ALL cells results in cessation of cellular proliferation and induction of T-cell differentiation. We performed dynamic global epigenomic and gene expression analyses to determine the role of Ikaros in tumor suppression during this process. Our results identified novel Ikaros functions in the epigenetic regulation of gene expression: Ikaros directly regulates de novo formation and depletion of enhancers, as well as de novo formation of active enhancers and activation of poised enhancers; Ikaros directly induces the formation of super-enhancers; and Ikaros demonstrates pioneering activity by directly regulating chromatin accessibility. Dynamic analyses demonstrate the long-lasting effect of Ikaros DNA binding on enhancer activation, de novo formation of enhancers and super-enhancers, and chromatin accessibility. Ikaros induces profound, global re-distribution of HDAC1 via recruitment of HDAC1 to promoter and enhancer regions of different target genes. Expression analysis identified a large number of novel signaling pathways that are directly regulated by Ikaros and Ikaros-induced enhancers, and that are responsible for the cessation of proliferation and induction of T-cell differentiation in T-ALL cells.
2019-03-31 | GSE126567 | GEO
Project description:Ikaros encodes a transcription factor that functions as a tumor suppressor in T-ALL. The mechanisms through which Ikaros regulates gene expression and cellular proliferation in T-ALL are unknown. Re-introduction of Ikaros into Ikaros-null T-ALL cells results in cessation of cellular proliferation and induction of T-cell differentiation. We performed dynamic global epigenomic and gene expression analyses to determine the role of Ikaros in tumor suppression during this process. Our results identified novel Ikaros functions in the epigenetic regulation of gene expression: Ikaros directly regulates de novo formation and depletion of enhancers, as well as de novo formation of active enhancers and activation of poised enhancers; Ikaros directly induces the formation of super-enhancers; and Ikaros demonstrates pioneering activity by directly regulating chromatin accessibility. Dynamic analyses demonstrate the long-lasting effect of Ikaros DNA binding on enhancer activation, de novo formation of enhancers and super-enhancers, and chromatin accessibility. Ikaros induces profound, global re-distribution of HDAC1 via recruitment of HDAC1 to promoter and enhancer regions of different target genes. Expression analysis identified a large number of novel signaling pathways that are directly regulated by Ikaros and Ikaros-induced enhancers, and that are responsible for the cessation of proliferation and induction of T-cell differentiation in T-ALL cells.
2019-03-31 | GSE126391 | GEO
Project description:Ikaros tumor suppression and epigenetic regulation [gene expression]
| PRJNA521762 | ENA
Project description:Ikaros tumor suppression and epigenetic regulation [ChIP-seq]
| PRJNA522415 | ENA
Project description:Ikaros tumor suppression and epigenetic regulation [ATAC-seq]
| PRJNA522416 | ENA
Project description:The IKZF1 gene encodes IKAROS – a DNA binding protein that acts as a tumor suppressor in T-cell acute lymphoblastic leukemia (T-ALL). IKAROS can act as a transcriptional repressor via chromatin remodeling, however the mechanisms through which Ikaros exerts its tumor suppressor function via heterochromatin in T-ALL are largely unknown. We studied human and mouse T-ALL using loss-of-function and Ikzf1 re-expression approach, along with Ikzf1-wildtype primary human and mouse T-ALL and thymocytes to establish the role of Ikaros and Ikaros-associated protein histone deacetylase 1 (HDAC1) in global regulation of facultative heterochromatin and transcriptional repression in T-ALL. Results identified novel Ikaros and HDAC1 functions in T-ALL: Ikaros and HDAC1 are essential for EZH2 histone methyltransferase activity, and formation of facultative heterochromatin; Recruitment of HDAC1 by Ikaros is critical for establishment of H3K27me3 and repression of active enhancers; and Ikaros-HDAC1 complexes promote formation and expansion of H3K27me3 large organized chromatin lysine domains (LOCKs) and broad genic repression domains (BGRDs) in T-ALL. Our results establish that Ikaros’ tumor suppressor function in T-ALL occurs via activation of EZH2 and HDAC1 function, global regulation of the facultative heterochromatin landscape and silencing of active enhancers that regulate oncogene expression.
2024-10-01 | GSE261181 | GEO